Occult hepatitis B (OBI) can

be associated Selleck Pifithrin �� with a chronic hepatitis C virus (HCV) infection. Even in the absence of serological markers of hepatitis B, some patients in the study had OBI, which may have affected their treatment response. Cacciola et al.11 studied 200 patients with a chronic HCV infection. In their study, they found that an OBI virus infection was more common (33%) in HCV patients versus controls, and this association might have affected the treatment response with interferon therapy. We wonder if they have additional data about the serological status of the patients with respect to their OBI status. In conclusion, the study performed by Harrison et al.1 will certainly broaden our horizons with respect to the treatment of chronic HCV. However, we would like to share our concerns about the study, and we hope to have a scientific discussion with the authors. Tugrul Purnak M.D.*, Cumali Efe Regorafenib in vitro M.D.†, Yavuz Beyazit M.D.‡, Ersan Ozaslan M.D.*,

* Department of Gastroenterology, Ankara Numune Education and Research Hospital, Ankara, Turkey, † Department of Internal Medicine, Bitlis Government Hospital, Bitlis, Turkey, ‡ Department of Gastroenterology, Yuksek Ihtisas Training and Research Hospital, Ankara, Turkey. “
“Primary liver cancer encompasses both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC). The Notch signaling pathway, known to be important for the proper development of liver architecture, is also a potential driver of primary liver cancer. However, with four known Notch receptors and several Notch ligands, it is not clear which Notch pathway members play the predominant role in

liver cancer. To address this question we utilized antibodies to specifically target Notch1, Notch2, Notch3 or Jag1 in a mouse model of primary liver cancer driven by AKT and NRas. We show that inhibition of Notch2 reduces tumor burden by eliminating highly malignant hepatocellular carcinoma- and cholangiocarcinoma-like tumors. Inhibition of the Notch ligand Jag 1 had a similar effect, triclocarban consistent with Jag1 acting in cooperation with Notch2. This effect was specific to Notch2, as Notch3 inhibition did not decrease tumor burden. Unexpectedly, Notch1 inhibition altered the relative proportion of tumor types, reducing HCC-like tumors but dramatically increasing CC-like tumors. Finally, we show that Notch2 and Jag1 are expressed in, and Notch2 signaling is activated in, a subset of human HCC samples. Conclusions: These findings underscore the distinct roles of different Notch receptors in the liver and suggest that inhibition of Notch2 signaling represents a novel therapeutic option in the treatment of liver cancer. (Hepatology 2014;) “
“In the February 2013 issue of Hepatology, in the Clinical Observations article entitled “Flipping the switch” (volume 57, pages 851-852; doi: 10.1002/hep.26193), by Rishi Agarwal, Joseph Buell, and Nathan J.